The long-term goal of biomaterials research lies in tissue regeneration, not replacement. In ‘tissue engineering’ biocompatible structures can be used either to engineer in-vitro living cellular constructs for transplantation, or to temporarily support load and facilitate in-vivo mechanisms for tissue regeneration. The ideal material for these purposes should provide high strength initially, then gradually degrade, transferring mechanical loads to regenerating tissue. Typical surgical applications are in the repair of connective soft tissue, ligaments or tendons and hard tissue such as bone.
In applications where tissue only requires temporary support or fixation the use of bioabsorbable polymers is appropriate. Depending on the choice of material and processing conditions, bioabsorbable polymers may retain their tissue supporting properties for days, weeks or months. Advantages of these materials are firstly, reduced risk of long-term complications because stresses are eventually transferred to the healing tissue, and secondly, the avoidance of the necessity for a retrieval operation.
Current trends in orthopaedic practice and research suggest that the most important bioabsorbable polymers used in surgery are synthetic polymers such as aliphatic polyesters (e.g. polyglycolide (PGA), polylactide (PLA) and their copolymers). These polyesters degrade in-vivo by hydrolysis into lactic acid and glycolic acid, which are then incorporated in the tricarboxylic acid cycle and excreted. These types of polymer generally degrade by bulk erosion, as the rate at which water penetrates the material exceeds the rate at which chain scission (into water-soluble fragments) occurs within the polymer [Middleton, J. C., Tipton, A. J., Biomaterials, 2335-2346, 2000]. Degradation in the interior of the device may occur faster than on the surface due to autocatalysis. The implication of this is that the device remains as a space-filler long after the useful strength of the polymer has deteriorated. The ingrowth of natural tissue is prevented, and a ‘lactide-burst’ of low pH material may be released when the surface of the implant is finally degraded which can damage surrounding cells and cause inflammation.